Understanding the Molecular Basis of Salt Sequestration in Epidermal Bladder Cells of Chenopodium quinoa

Soil salinity is destroying arable land and is considered to be one of the major threats to global food security in the 21st century. Therefore, the ability of naturally salt-tolerant halophyte plants to sequester large quantities of salt in external structures, such as epidermal bladder cells (EBCs), is of great interest. Using Chenopodium quinoa, a pseudo-cereal halophyte of great economic potential, we have shown previously that, upon removal of salt bladders, quinoa becomes salt sensitive. In this work, we analyzed the molecular mechanism underlying the unique salt dumping capabilities of bladder cells in quinoa. The transporters differentially expressed in the EBC transcriptome and functional electrophysiological testing of key EBC transporters in Xenopus oocytes revealed that loading of Na+ and Cl− into EBCs is mediated by a set of tailored plasma and vacuole membrane-based sodium-selective channel and chloride-permeable transporter. Böhm et al. report that the inward-rectifier CqHKT1.2 is a key player for the Na+ load into bladder cells under salinity stress. Together with transporters for compatible solutes, these transport systems mediate sequestration of salt into bladders, arming quinoa with an efficient mechanism to protect the metabolically active photosynthetic tissues.